| Objective: To observe the intestinal tissue injury, epithelial cellsapoptosis and the changes of GRP78expression in the intestineischemia-reperfusion rats, and to investigate the possible effect andmechanism of intestinal apoptosis and endoplasmic reticulum stress in theischemic process.Methods: Forty-five Sprague Dawleys were randomly divided into9groups: sham control group and0hours,1hour,3hour,6hour,12hour,24hour,48hour and72hour after ischemia reperfusion groups,5rats in eachgroup. An experimental model of intestinal ischemia-reperfusion in rats wasestablished by the occlusion of superior mesenteric artery for1hour by smallatraumatic clip, and sham control animals were prepared in the same waywithout the occlusion of a.mesenterica. Intestinal tissue injury severity of ratwas tested by HE assay. The apoptosis of epithelial cells was measured byTUNEL method. The expression of GRP78in intestinal tissue was detectedby Western blot and RT-PCR..Results: HE assay and TUNEL showed that the tissue injury andapoptotic index of intestinal mucosa were gradually elevated with increasing time of reperfusion, and they reached a peak at3hour（compared with othergroups, P <0.05）, fell to the level of the control groups at72hour. Theexpression of GRP78was increased after reperfusion, reached a first smallpeak at1hour（compared with0h and3h group, P <0.05）, but droppeddown with the reperfusion time prolongation, rose again at12hour（compared with6hgroup,P<0.004）,peakedagainat24hour（comparedwith other groups, P <0.05）, and fell to the level of the control groups（compared with control group, P>0.069）at72hour.Conclusion: The endoplasmic reticulum stress initiated by intestineischemia-reperfusion, which induced the apoptosis of epithelial cells with anintrinsic route. And the changes of GRP78expression might be concernedwith the endogenous protective mechanisms in intestineischemia-reperfusion injury. |
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